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ChIP-seq for beta-catenin, EZH2, EED, KMT2B, H3K4me3, H3K27me3 and sequential chipseq

ABSTRACT: Genome-wide measurements of histone modifications and transcripton factors binding in different prostate cancer clinical tumors tissue, PDX tumor, and cell models to study the tumor lineage plasticity and chromatin bivalency.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE294966 | GEO | 2026/02/28

REPOSITORIES: GEO

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ChIP-seq for beta-catenin, EZH2, EED, KMT2B, H3K4me3, H3K27me3 and sequential chipseq

Project description:ChIP-seq for beta-catenin, EZH2, EED, KMT2B, H3K4me3, H3K27me3 and sequential chipseq

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H3K4me3/H3K27me3 bivalent chromatin function to fine-tune gene expression level

Project description:Bivalency, the paradoxical juxtaposition of transcriptionally activating trimethylation of histone H3 lysine 4 (H3K4me3) and the repressive trimethylation of histone H3 lysine 27 (H3K27me3), has been proposed to decorate developmental genes poised for gene expression regulation. Here, we report development of sequential internally calibrated chromatin immunoprecipitation (Re-ICeChIP-seq), capable of measuring absolute quantities of nucleosomal patterns of histone marks in a genome-wide fashion, combined with in situ control of antibody specificity. Re-ICeChIP-seq of H3K4me3/H3K27me3 in mESC reveals that bivalent genes can be delineated into two classes, distinguished by the nucleosomal ratio of H3K4me3 to H3K27me3. Consistent with the canonical role of bivalency, H3K27me3-rich bivalent nucleosomes demarcate promoters of poorly expressed developmental genes that may be poised for activation or repression. Yet our measurements reveal surprisingly widespread presence of bivalency at promoters of highly-expressed housekeeping genes, characterized by H3K4me3-rich bivalent nucleosomes. Moreover, the ratio of H3K4me3 to H3K27me3 at transcription start sites better correlates with gene expression than H3K4me3 or H3K27me3 alone, suggesting cooperation between opposing marks to fine-tune gene expression. Finally, we report that major H3K4 methyltransferases exhibit wide acceptance of various H3K27me3 substrates.

2021-01-04 | GSE108747 | GEO

Individual ChIP-seq for BRD4 and H3K27ac

Project description:Genome-wide measurements of histone modifications and transcripton factors binding in Luca145.2 PDX tumor and 42D cell models to studyBRD4 and H3K27ac regulate the tumorigenic programs

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Individual ChIP-seq for REV-ERBα, FOXA1,BRD4 and H3K27ac

Project description:Genome-wide measurements of histone modifications and transcripton factors binding in Lucao35CR PDX tumor and cell models to study FOXA and REV-ERBα regulate the tumorigenic programs

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reChIP-seq reveals widespread bivalency of H3K4me3 and H3K27me3 in CD4+ memory T-Cells

Project description:Identification of genomic loci exhibiting the physical co-localization of two distinct DNA-associated proteins remains a technical challenge. To tackle this challenge we have developed a novel reChIP-seq approach that enriches for two distinct DNA-associated proteins in an unbiased and genome-wide manner. We illustrate the utility of our approach by identifying nucleosomes bivalently modified by H3K4me3 and H3K27me3 in primary human CD4+ central memory T-cells (TCMs). We unravel widespread bivalency of many unmethylated CpG-rich regions in TCMs overlapping with transcriptional start sites of developmental regulators. Furthermore, reChIP-seq uncovers two yet unobserved classes of bivalency, where either H3K4me3 or H3K27me3 is mixed with low but detectable bivalency. We provide evidence that bivalency is established by an interplay between genome and epigenome and thus attains stability. Our described reChIP-seq approach augments conventional ChIP-seq and is broadly applicable in the study of co-localization of DNA-associated proteins to unravel the intricate possibilities of combinatorial action.

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EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent.

Project description:In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PRC2 writing of H3K27me3 is mechanistically required for gene silencing. Here, we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (embryonic ectoderm development) inactivation in the postnatal heart (EedCKO) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in EedCKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized EedCKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.

| S-EPMC5400508 | biostudies-literature

Genome wide mapping of H3K4me3 and H3K27me3 marks in trophoblast progenitors derived from human embryonic stem cells

Project description:Human embryonic stem cells (hESC) can be differentiated into progenitors resembling trophoblast upon exposure to BMP4. Putative trophpblast progenitors express APA cell surface marker Using trophoblast progenitors at day 2.5 of BMP4-induced differentiation, here we profile H3K4me3 and H3K27me3 chromatin marks that mark active and inactive genes, respectively. Double occupancy indicates bivalency

2017-10-20 | GSE105258 | GEO

ChIPseq for H3K4me3 and H3K27me3 in LT-HSCs and MPPs

Project description:The distribution of H3K4- and H3K27me3 on the chromatin of mouse longterm hematopoietic stem cells and multipotent progenitor cells has been profiled by ChIP-seq.

2021-11-02 | E-MTAB-10661 | biostudies-arrayexpress

Project description:Neurons are central to lifelong learning and memory, but ageing disrupts their morphology and function, leading to cognitive decline. Although epigenetic mechanisms are known to play crucial roles in learning and memory, neuron-specific genome-wide epigenetic maps into old age remain scarce, often being limited to whole-brain homogenates and confounded by glial cells. Here, we mapped H3K4me3, H3K27ac, and H3K27me3 in mouse neurons across their lifespan. This revealed stable H3K4me3 and global losses of H3K27ac and H3K27me3 into old age. We observed patterns of synaptic function gene deactivation, regulated through the loss of the active mark H3K27ac, but not H3K4me3. Alongside this, embryonic development loci lost repressive H3K27me3 in old age. This suggests a loss of a highly refined neuronal cellular identity linked to global chromatin reconfiguration. Collectively, these findings indicate a key role for epigenetic regulation in neurons that is inextricably linked with ageing.

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Dual recognition of H3K4me3 and H3K27me3 by a plant histone reader SHL.

Project description:The ability of a cell to dynamically switch its chromatin between different functional states constitutes a key mechanism regulating gene expression. Histone mark "readers" display distinct binding specificity to different histone modifications and play critical roles in regulating chromatin states. Here, we show a plant-specific histone reader SHORT LIFE (SHL) capable of recognizing both H3K27me3 and H3K4me3 via its bromo-adjacent homology (BAH) and plant homeodomain (PHD) domains, respectively. Detailed biochemical and structural studies suggest a binding mechanism that is mutually exclusive for either H3K4me3 or H3K27me3. Furthermore, we show a genome-wide co-localization of SHL with H3K27me3 and H3K4me3, and that BAH-H3K27me3 and PHD-H3K4me3 interactions are important for SHL-mediated floral repression. Together, our study establishes BAH-PHD cassette as a dual histone methyl-lysine binding module that is distinct from others in recognizing both active and repressive histone marks.

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